Abstract
Salidroside (SAL) is the major pharmacologically active constituent of Rhodiola rosea, which possesses a wide range of pharmacological functions, including anti-aging, anti-inflammatory, antioxidant, anticancer and neuroprotective activities. However, the effects and mechanisms of SAL on oxidative stress in retinal pigment epithelial (RPE) cells exposed to hydrogen peroxide (H(2)O(2)) remain unclear. The present study investigated the protective effects of SAL and the underlying mechanisms against H(2)O(2)-induced oxidative stress in human RPE cells. ARPE-19 cells were treated with various doses of SAL for 24 h and then exposed to 200 µM H(2)O(2) for 24 h. Cell viability was analyzed by a MTT assay, and the intracellular levels of reactive oxygen species were measured using CellROX orange reagent. Cell apoptosis was analyzed by annexin V/propidium iodide double staining, followed by flow cytometry. The levels of B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein, phospho (p)-protein kinase B (Akt), Akt, p-glycogen synthase kinase (GSK)-3β and GSK-3β were evaluated using western blotting. The results demonstrated that SAL markedly attenuated H(2)O(2)-induced loss of cell viability. SAL also ameliorated H(2)O(2)-induced oxidative stress and cell apoptosis in RPE cells. In addition, pretreatment with SAL significantly increased the phosphorylation levels of Akt and GSK-3β in H(2)O(2)-treated ARPE-19 cells. In conclusion, the present study demonstrated that SAL protected RPE cells against H(2)O(2)-induced cell injury through the activation of the Akt/GSK-3β signaling pathway. This suggests that SAL may be a potential therapeutic strategy for the treatment of age-related macular degeneration.